Topic: Watch out this over 1 million $ grant to STEERE
Dave6002
Frequent Contributor (1K+ posts)
Member # 9064
posted
Abstract Grant Number: 2R01AR020358-32A1 PI Name: STEERE, ALLEN C. PI Email: [email protected] PI Title: CHIEF Project Title: Lyme Arthritis: A New Epidemic Disease
Lyme disease, which is caused by the tick-borne
spirochete Borrelia burgdorferi, can usually be
treated successfully with 2-4 week courses of
oral or intravenous antibiotic therapy. However,
~10% of patients with Lyme arthritis have
persistent synovial inflammation despite such
courses of therapy. To explain
antibiotic-refractory Lyme arthritis after 2-3
month courses of oral and IV antibiotics, the
competing hypotheses of persistent infection or
infection-induced autoimmunity have been proposed.
In the absence of an animal model, clinical
correlations in human patients are required to
address these hypotheses. To date, most patients
with antibiotic-refractory Lyme arthritis have had
negative PCR results for B. burgdorferi DNA in
joint fluid after antibiotic treatment; they have
had HLA-DRB molecules that bind the OspA163-i75
epitope of the spirochete, particularly the
DRB1*0401, 0404 and 0101 molecules, and T cell
reactivity with this epitope. Our goals in the
next grant cycle include an assessment of antibody
responses to lipid and carbohydrate antigens of
B. burgdorferi to determine whether a decline in
one of these responses after antibiotic therapy
might serve as a practical surrogate marker for
spirochetal killing in Lyme disease. The
precursor frequencies of T cells specific for
OspA163-i75 or implicated autoantigens will be
determined in both the infectious and
post-antibiotic periods of the illness, the clonal
characteristics of these cells will be
delineated, and the numbers and function of T
regulatory cells will be determined during active
arthritis through arthritis resolution. To
broaden the search for candidate autoantigens
beyond those identified by sequence homology with
the OspA-,63-175 epitope, B cell epitopes of
putative autoantigens will be sought using patient
sera to screen a large array of expressed human
proteins, and T cell epitopes will be sought using
patient synovial tissue as a source of naturally
processed MHC complexes from which peptides will
be eluted and identified using tandem mass
spectrometry. The knowledge gained from these
studies is likely to aid in more accurate
diagnosis and more effective treatment of
antibiotic-refractory Lyme arthritis. Of greater
general importance, antibiotic-refractory Lyme
arthritis, which shares similar HLA associations
with rheumatoid arthritis, may serve as a model of
infection-induced autoimmunity. Furthermore, this
work brings us closer to the long-term goal of
direct comparisons of antigens in Lyme arthritis
and rheumatoid arthritis synovia
Thesaurus Terms: Lyme disease, arthritis, autoantigen, autoimmune disorder, bacterial antigen, genetic susceptibility, leukocyte adhesion molecule, pathologic process Borrelia, T lymphocyte, antirheumatic agent, arthritis therapy, disease /disorder proneness /risk, drug resistance, human population genetics, human therapy evaluation, major histocompatibility complex human subject, patient oriented research, synovial fluid
Institution: MASSACHUSETTS GENERAL HOSPITAL 55 FRUIT ST BOSTON, MA 02114 Fiscal Year: 2006 Department: Project Start: 01-JUL-1987 Project End: 31-JUL-2011 ICD: NATIONAL INSTITUTE OF ARTHRITIS AND MUSCULOSKELETAL AND SKIN DISEASES IRG: ACTS
posted
You noticed the project start and finish dates? Just going on forever, isn't it?
His mind is made up already. Just count the number of times autoantigens is used in this description. Autoimmunity is the only answer he is prepared to accept for the "post antibiotic" symptoms. These would be symptoms that occurred after mostly inadequate treatment.
We would be better off with grants that supported research to find out why scientists/doctors fail to use the scientific method in forumlating hypotheses. And to establish a school for remedial treatment of said scientists/doctors.
Posts: 8430 | From Not available | Registered: Oct 2000
| IP: Logged |
Truthfinder
Frequent Contributor (1K+ posts)
Member # 8512
posted
Well, since there are NO reliable tests to detect Bb in blood or tissues, what are they going to use to determine a "persistent infection"?
That is a key factor here, and testing methods are rarely in much detail in these "tainted" studies.
By the way, I could only read part of this since it is in one big block of text.
Tracy
-------------------- Tracy .... Prayers for the Lyme Community - every day at 6 p.m. Pacific Time and 9 p.m. Eastern Time � just take a few moments to say a prayer wherever you are�. Posts: 2966 | From Colorado | Registered: Dec 2005
| IP: Logged |
Dave6002
Frequent Contributor (1K+ posts)
Member # 9064
posted
I agree with that there could be autoimmune involved in Lyme and it's very likely as in the case of MS.
However, I don't believe the autoimmune is the root of the Lyme disease or the Lyme Arthritis as described in this grant.
Rather chronical infections is the culpits of these diseases. Once these pathogens have been eradicated, these symptoms including autoimmune will be resolved.
Dr. Steere missed the target. He contended that Lyme arthritis have had negative PCR results for B. burgdorferi DNA in joint fluid after antibiotic treatment. This could be true, but cannot exclude the possibilities (very likely) that (1) B. burgdorferi could exist in other tissues especially the brain. (2)There could be other pathogens that co-transmitted (co-infections) by ticks that cause Lyme Arthritis, and we know that coinfections are very commona moung Lymes.
The almost true concept that MS is an autoimmune is losing its ground to the hypothesis that MS is caused by chronical infections.
To label chronical Lyme disease as autoimmune disease is totally wrong.
People should focus on how to find the pathogens in the patients and how to eradicat them.
Dave
Posts: 1078 | From Fairland | Registered: Apr 2006
| IP: Logged |
klutzo
Frequent Contributor (1K+ posts)
Member # 5701
posted
Just my opinion, but I think he has dug himself a hole that goes all the way to China!
After 21 yrs. of reading research and talking to doctors off the record at seminars and when they spoke at the support group I used to run, I am convinced that "auto-immunity" is just arrogant medico-speak for "we have no friggin' idea what is going on".
I do not believe the human immune system is that dumb, therefore, I do not believe in auto-immunity until proven otherwise.
Want an example? Research the history of tuberculosis, which was originally thought to be several different diseases, and all of them were assumed to be auto-immune. Sound familiar? (FMS, CFS, ALS, MS, AZD and Lyme???)
IMO, diseases are only considered autoimmune until they finally discover the REAL cause. In the case of TB it is a spirochete.....hmmm....you'd think they would have learned from that....
Klutzo
Posts: 1269 | From Clearwater, Florida, USA | Registered: May 2004
| IP: Logged |
posted
Were you thinking of syphilis and spirochetes, klutzo, not TB which is not a spirochetal disease? Perhaps a "lyme brain" moment, of which I have many also.
Maybe there really is such a thing as autoimmunity but like the posters above, am very skeptical that it has been the label slapped on diseases they don't understand. When they round up the usual suspects, it generally is genetics and autoimmunity or both! This saves the embarrasssing admission that experts don't have all the answers.
And on the pcr of synovial fluid....wasn't there a study that showed it was more apt to be found in synovial tissue rather than fluid? But if you don't want to find something, you go where it isn't!
Posts: 8430 | From Not available | Registered: Oct 2000
| IP: Logged |
Michelle M
Frequent Contributor (1K+ posts)
Member # 7200
posted
Lyme arthritis. Spirochetes found in synovial microangiopathic lesions. (1985)
* Johnston YE, * Duray PH, * Steere AC, * Kashgarian M, * Buza J, * Malawista SE, * Askenase PW.
In 17 patients with Lyme disease, synovial specimens, obtained by synovectomy or needle biopsy, showed nonspecific villous hypertrophy, synovial cell hyperplasia, prominent microvasculature, lymphoplasmacellular infiltration, and sometimes lymphoid follicles.
The larger surgically obtained specimens also showed striking deposition of fibrin in synovial stroma and a form of endarteritis obliterans.
In 2 patients, spirochetes were seen in and around blood vessels by the Dieterle silver stain. Compared with 55 cases of other synovial disease, obliterative microvascular lesions were seen only in Lyme synovia, but marked stromal deposition of fibrin seemed nonspecific.
These findings imply that the Lyme spirochete may survive for years in affected synovium and may be directly responsible for the microvascular injury.
PMID: 3966535 [PubMed - indexed for MEDLINE] __________________________________________________
It must pain Dr. Steere that he cannot UNpublish these embarassing earlier "discoveries."
It is kind of amazing that the government continues handing out millions to discover things that have already been amply discovered.
Michelle
Posts: 3193 | From Northern California | Registered: Apr 2005
| IP: Logged |
tdtid
Frequent Contributor (1K+ posts)
Member # 10276
posted
As with many of you I'm sure.....this kind of thing makes my blood boil.
Why keep tossing good money in Steere's direction? Wouldn't it make more sense to them to use it in research, maybe something like Columbia or Dr. Fallon or the likes of someone that may be making progress?
This is all just so darn frustrating. Not good. Not good at all!
Cathy
-------------------- "To Dream The Impossible Dream" Man of La Mancha Posts: 2638 | From New Hampshire | Registered: Oct 2006
| IP: Logged |
Dave6002
Frequent Contributor (1K+ posts)
Member # 9064
posted
I was wondering why NIH cannot incorporate comsumers(Lyme patients)into their grant review process as the DOD (Department of Defense) has been doing.
Posts: 1078 | From Fairland | Registered: Apr 2006
| IP: Logged |
klutzo
Frequent Contributor (1K+ posts)
Member # 5701
posted
Hi Lou, Thank you for correcting me. I cannot blame this one on Lyme brain. I can blame it on the ARNP in Rheumatology who told me the story of tuberculosis, and first got me thinking about whether autoimmunity is real or not.
She is the one who told me it was caused by a spirochete. I just Googled it, and of course, you are right, it is a bacterium. Shame on her,to get that wrong with all that education.
I am glad you were still able to discern my point, in spite of my big boo-boo!
Klutzo
Posts: 1269 | From Clearwater, Florida, USA | Registered: May 2004
| IP: Logged |
posted
Dave, I suggested just that very thing to NIH some time ago when the subject of peer review for grant applications was raised in a science journal. Just full of good suggestions, am I. But it ain't gonna happen. This is the good old boys using our money in ways that improve their standard of living, but not necessarily our health. Having patient input would gum up their slick self serving system.
Good find on the Steere article, Michelle. Don't you wish we could get these guys up in front of a panel of patients so we could grill them. Sir, what did you mean in your 1985 article, and how does that correspond with your more recent opinions on the subject?????
[ 07. January 2007, 05:35 PM: Message edited by: lou ]
Posts: 8430 | From Not available | Registered: Oct 2000
| IP: Logged |
-------------------- The best index to a person's character is how he treats people who can't do him any good, and how he treats people who can't fight back. -Abigail van Buren (Pauline Esther Friedman) (1918-2002) Posts: 409 | From Florida | Registered: Dec 2005
| IP: Logged |
posted
Hi, Maybe this article along wtih Michelle's should be sent to the CT Atty. General???
It's good that we are aware of it, but if you give it to someone with power enough to make change, alll the better for everyone!
Kayda
Posts: 582 | From midwest | Registered: Nov 2006
| IP: Logged |
Michelle M
Frequent Contributor (1K+ posts)
Member # 7200
posted
quote:Originally posted by lou: Good find on the Steere article, Michelle. Don't you wish we could get these guys up in front of a panel of patients so we could grill them. Sir, what did you mean in your 1985 article, and how does that correspond with your more recent opinions on the subject?????
Well, there seems to be an intriguing difference in position here...
THEN:"The lyme spirochete might survive for years" (1985)
and
NOW: 'Any studies documenting so-called 'persistence' of the bacteria must be the result of cross-contamination in the lab.' (new IDSA guidelines, paraphrased; don't have them handy]
Yep, every single study showing persistence (there's at least a dozen good ones) must've been "cross-contaminated in the lab," despite being in various labs and settings and periods of time.
Uh, yeah, that's it.
Steere is an embarrassment. I don't know how anyone can pretend to believe him. If I were an IDSA colleague of his, I'd get a tee shirt that says "I'm not with stupid."
Michelle
Posts: 3193 | From Northern California | Registered: Apr 2005
| IP: Logged |
northstar
Frequent Contributor (1K+ posts)
Member # 7911
posted
So,
if previous results are faulty due to hypothesized cross contamination,
then the same probability may apply to current studies,
e.g. sloppy lab work, poor quality control, slack oversight of methodology and materials handling, etc.
Therefore, all his studies are potentially invalid/tainted, even new ones.
Why does he keep shooting himself in the foot?
Northstar
Northstar
Posts: 1331 | From hither and yonder | Registered: Sep 2005
| IP: Logged |
posted
Someone very astutely pointed out that the over one million dollar grant began in 1987 and will end in 2011. Was the grant extended this year for another million? Can't figure it out.
**Institution: MASSACHUSETTS GENERAL HOSPITAL 55 FRUIT ST BOSTON, MA 02114 Fiscal Year: 2006 Department: Project Start: 01-JUL-1987 Project End: 31-JUL-2011 ICD: NATIONAL INSTITUTE OF ARTHRITIS AND MUSCULOSKELETAL AND SKIN DISEASES IRG: ACTS
Nan
[ 08. January 2007, 11:40 AM: Message edited by: nan ]
-------------------- nan Posts: 2135 | From Tick Country | Registered: Oct 2000
| IP: Logged |
Dave6002
Frequent Contributor (1K+ posts)
Member # 9064
posted
For this kind of grants, the period is usually five years and the fund is usually over 1 million dollars. After five year term is done, you could renew the grant and get another over 1 million for another five years. This process can goe this way forever.
From 1977 to 2011, that's 34 years, about five 7 years,this means that Dr. Steere has been awarded at least seven million direct cost on this project. NIH also gives about 40% indirect cost as overheads. So the totall moneey would over 10 million dollars.
Foggy
Frequent Contributor (1K+ posts)
Member # 1584
posted
Folks, this is why the Columbia Lyme Reseach center is SO important!
They could recieve similar grants.
Notice how this doesn't address cases where a patient tests PCR - prior to abx, then PCR + after lt abx...
24 years & millions of our tax $ & they still have no better treatments than lt abx!?
Posts: 2451 | From Lyme Central | Registered: Aug 2001
| IP: Logged |
Dave6002
Frequent Contributor (1K+ posts)
Member # 9064
posted
Grant 2001 to 2006:
Grant Number: 2R01AR020358-26 PI Name: STEERE, ALLEN C. PI Email: [email protected] PI Title: CHIEF Project Title: LYME ARTHRITIS- A NEW EPIDEMIC DISEASE
Abstract: DESCRIPTION: (Verbatim) - About 10 percent of patients with Lyme arthritis have persistent knee swelling for months or even several years after oral and intravenous antibiotic therapy. After treatment, such patients, in our experience, have no remaining spirochetal DNA in synovial tissue or joint fluid, suggesting that live spirochetes have been eliminated from the joint. During the past grant cycle, we identified a possible autoimmune mechanism that may partially explain the persistence of Lyme arthritis after antibiotic therapy. The mechanism in DRB1*0401-positive individuals involves molecular mimicry between the dominant T cell epitope of B. burgdorferi outer-surface protein A (OspA165-173) and a homologous sequence of human lymphocyte function associated antigen-1 (hLFA-1alpha332-340). In this proposal, we test the hypothesis that synovial inflammation may persist in treatment-resistant arthritis patients with a range of MHC alleles because of molecular mimicry between this dominant T cell epitope of OspA and hLFA-1. Our plan is to determine the frequencies of various MHC alleles in patients with treatment-resistant arthritis compared with those in treatment-responsive patients and those in a control population. PBL and synovial fluid lymphocytes (SFL) from treatment-responsive and treatment-resistant patients will be screened for reactivity with OspA165-173 and LFA-1alpha332-340, and cloned OspA165-173-reactive T cells from selected patients with a range of MHC alleles will be tested for reactivity with hLFA-1alpha332-340. Using an in vitro peptide binding assay, DR or DQ molecules obtained from selected patients' EBV-transformed B cells will be tested for their ability to bind the OspA and hLFA-1 peptides. Finally, after appropriate antibiotic treatment, the efficacy and safety of DMARD therapy will be observed in treatment-resistant patients. Lyme arthritis is the only human form of chronic inflammatory arthritis in which the triggering agent, immunogenetic susceptibility, and a candidate autoantigen are known. Thus, it is currently the only human system in which it is possible to explore specific infectious and autoimmune mechanisms that may lead to chronic inflammatory arthritis.
Thesaurus Terms: Lyme disease, arthritis, autoantigen, autoimmune disorder, bacterial antigen, genetic susceptibility, leukocyte adhesion molecule, pathologic process Borrelia, T lymphocyte, antirheumatic agent, arthritis therapy, disease /disorder proneness /risk, drug resistance, human population genetics, human therapy evaluation, major histocompatibility complex human subject, patient oriented research, synovial fluid
Institution: NEW ENGLAND MEDICAL CENTER HOSPITALS 750 WASHINGTON ST BOSTON, MA 021111533 Fiscal Year: 2001 Department: Project Start: 01-JUL-1987 Project End: 28-FEB-2006 ICD: NATIONAL INSTITUTE OF ARTHRITIS AND MUSCULOSKELETAL AND SKIN DISEASES IRG: GMA
Posts: 1078 | From Fairland | Registered: Apr 2006
| IP: Logged |
Dave6002
Frequent Contributor (1K+ posts)
Member # 9064
posted
1996 to 2001
Grant Number: 2R01AR020358-21A1 PI Name: STEERE, ALLEN C. PI Email: [email protected] PI Title: CHIEF Project Title: LYME ARTHRITIS--A NEW EPIDEMIC DISEASE
Abstract: This abstract is not available.
Thesaurus Terms:
There are no thesaurus terms on file for this project.
Institution: NEW ENGLAND MEDICAL CENTER HOSPITALS 750 WASHINGTON ST BOSTON, MA 021111533 Fiscal Year: 1996 Department: Project Start: 01-JUL-1987 Project End: 31-MAR-2001 ICD: NATIONAL INSTITUTE OF ARTHRITIS AND MUSCULOSKELETAL AND SKIN DISEASES IRG: GMA
Posts: 1078 | From Fairland | Registered: Apr 2006
| IP: Logged |
Dave6002
Frequent Contributor (1K+ posts)
Member # 9064
posted
1991 to 1996
Grant Number: 5R01AR020358-16 PI Name: STEERE, ALLEN C. PI Email: [email protected] PI Title: CHIEF Project Title: LYME ARTHRITIS: A NEW EPIDEMIC DISEASE
Abstract: Lyme disease is a tick-transmitted infection caused by a newly recognized Borrelia burgdorferi. The illness, which affects both children and adults, usually begins with a characteristic skin lesion, erythema migrans, which may be followed by meningitis, cranial or peripheral neuritis, myocarditis, or arthritis. Our work covers the natural history, diagnosis, treatment, epidemiology, and pathogenesis of this disorder. During the next granting period, studies of the natural history of the illness will be continued in patients with arthritis, CNS abnormalities, acrodermatitis chronica atrophicans, or maternal-fetal illness. Sensitive and specific diagnostic tests will be developed for early disease and for neurologic abnormalities, and clinically useful evidence for persistent immunologic and inflammatory stimulation will be sought through serial measurements in plasma of Interleukin-1 (and its endogenous inhibitors), C-reactive protein, and fibrinopeptide A. Antibiotic therapy regimens will be tested in patients with arthritis, and the role of arthroscopic synovectomy will be assessed in unresponsive cases. The frequency, duration, and risk of asymptomatic infection will be ascertained in defined populations. To further understand the pathogenesis of the arthritis, monoclonal antibodies will be generated against B. burgdorferi and against the idiotypes of anti-B. burgdorferi, which will be used to search for B. burdorferi in synovium, to look for evidence of molecular mimicry or peptidoglycan, and to explore the specificities of the immune response in this tissue. Spirochetal antigens will be sought within immune complexes in serum and joint fluid. An animal model for Lyme disease will be sought to further understand pathogenetic mechanisms. With collaborators, the frequency and role of certain autoantibodies will be defined, immunogenetic profiles will be determined using typing sera and alloreactive T cell clones, and lymphocyte-endothelial cell interactions will be investigated in synovium. This work will provide important information about the diagnosis and treatment of Lyme disease, and may have implications for other rheumatic diseases.
Institution: NEW ENGLAND MEDICAL CENTER HOSPITALS 750 WASHINGTON ST BOSTON, MA 021111533 Fiscal Year: 1991 Department: Project Start: 01-JUL-1987 Project End: 31-DEC-1991 ICD: NATIONAL INSTITUTE OF ARTHRITIS AND MUSCULOSKELETAL AND SKIN DISEASES IRG: GMA
Dave6002
Frequent Contributor (1K+ posts)
Member # 9064
posted
1985 to 1991
Grant Number: 5R01AM020358-09 PI Name: STEERE, ALLEN C. PI Email: [email protected] PI Title: CHIEF Project Title: LYME ARTHRITIS: A NEW EPIDEMIC DISEASE
Abstract: Lyme disease, a tick-transmitted, immune-mediated, spirochetal infection in children and adults, usually begins in summer with a characteristic skin lesion, erythema chronicum migrans, that may be followed weeks to months later by meningo-encephalitis, cranial or peripheral neuritis, myocarditis, or by migratory, intermittent or chronic arthritis. We plan to define the natural history, prognosis, treatment, epidemiology, etiology and pathogenesis of this illness. To accomplish these objectives, a network of physicians has been established to refer patients with the disease. The natural history of the disorder will be described from the serial examination of these patients. Antibiotic therapy regimens will be studied for each stage of the illness. Blood, cerebrospinal fluid, joint fluid, skin and synovial biopsy specimens from patients will be cultured for the I. dammini spirochete. Specific serologic tests will be developed for diagnosis, and the frequency of symptomatic and asymptomatic infection will be determined during consecutive summers in a stable, island population. Spirochetal antigen and antibody will be sought in immune complexes in serum and joint fluid, the effects of the causative agent and a serum factor upon lymphocyte function will be studied, and the inter-actions among the causative agent, immunogenetic determinants, circulating immune complexes and lymphocytes will be examined. To understand further the pathogenesis, an animal model for Lyme disease will be sought. This work will provide important information about the diagnosis and treatment of Lyme disease, and the studies of pathogenesis may have implications for other rheumatic diseases. In particular, the question of a persistent infectious agent being necessary for continued disease activity, as opposed to triggering by such an agent followed by autoimmunity, is of central importance in a number of rheumatic diseases.
Thesaurus Terms: BACTERIAL DISEASES, PLAGUE (YERSINIA PESTIS), COMMUNICABLE DISEASE TRANSMISSION, INVERTEBRATE VECTORS OF HUMAN DISEASE, GENERAL MEDICINE A STUDY SECTION, VIRUS DISEASES ARTHROPODS, ARACHNIDS, TICKS, BACTERIAL DISEASES, SPIROCHETAL DISEASES, LYME DISEASE, HEART DISORDERS, MYOCARDITIS, IMMUNITY, HUMORAL IMMUNITY, IMMUNOGENETICS (GENERAL), IMMUNOLOGICAL TESTS AND IMMUNOASSAY, IMMUNOLOGICAL TESTS, IMMUNOLOGY, MICROBIAL, IMMUNOPATHOLOGY, IMMUNE COMPLEX DISEASES (SEE ALSO SPECIFICS), NERVOUS DISORDERS CENTRAL (GENERAL), NERVOUS DISORDERS CENTRAL, MENINGOENCEPHALITIS EOSINOPHILIC, NERVOUS DISORDERS PERIPHERAL, NEURITIS, POPULATION STUDIES HUMAN, EPIDEMIOLOGY, SKELETAL DISORDERS DIAGNOSIS (INCL EXAMS), SKELETAL DISORDERS, ARTHRITIS, SKELETAL DISORDERS, JOINT DISORDERS, SKIN DISORDERS, ERYTHEMA (GENERAL), communicable disease control HUMAN, CLINICAL, IMMUNOLOGICAL TESTS AND IMMUNOASSAY, IMMUNOFLUORESCENCE, IMMUNOLOGICAL TESTS AND IMMUNOASSAY, RADIOIMMUNOASSAY, MAMMALS, ARTIODACTYLA, SWINE, MAMMALS, CARNIVORES, DOGS, MAMMALS, LAGOMORPHS, MAMMALS, PRIMATES, MONKEYS AND APES, MAMMALS, RODENTS, MYOMORPHA, MICE (LABORATORY), OPTICS, MICROSCOPY, ELECTRON, TISSUE (CELL) CULTURE
Institution: YALE UNIVERSITY 47 COLLEGE STREET, SUITE 203 NEW HAVEN, CT 065208047 Fiscal Year: 1985 Department: Project Start: 15-SEP-1977 Project End: 31-DEC-1986 ICD: NAT INST OF ARTHRITIS, DIABETES, DIGESTIVE & KIDNEY DISEASES IRG: GMA
Posts: 1078 | From Fairland | Registered: Apr 2006
| IP: Logged |
Dave6002
Frequent Contributor (1K+ posts)
Member # 9064
posted
Grant Number: 1R01AM020358-01 PI Name: STEERE, ALLEN C. PI Email: [email protected] PI Title: CHIEF Project Title: LYME ARTHRITIS: A NEW EPIDEMIC DISEASE
Abstract: We have recently uncovered a new, epidemic disease -- Lyme arthritis -- probably caused by a tick-transmitted virus in which immune complex formation is associated with lesions in the skin, joints, heart, or central nervous system. We plan to define the natural history of this illness -- its course and prognosis -- etiology, vector, and pathogenesis. To accomplish these objectives, a network of primary physicians has been established to refer patients with erythema chronicum migrans and/or Lyme arthritis. The natural history of the illness will be described from the serial examination of these patients. Cryoprecipitates will be sought for in the sera of each patient at each visit, and characterized. Specimens from patients will be inoculated into tissue cultures, and skin, synovial, and cryoprecipitate specimens will be examined by electronmicroscopy. Ticks collected in the field will be identified by species, pooled, and extracts inoculated into tissue cultures and mice. Extracts from tick pools will be reacted with convalescent sera in double immunodiffusion gels and by immunoelectronmicroscopic techniques. If a serologic test can be developed for Lyme arthritis, positive diagnosis will be possible in all affected patients, and studies will be conducted in the epidemic area and in other areas, to determine attack rates within sample human and animal populations; the results would provide the basis for decisions about control measures.
The Lyme Disease Network is a non-profit organization funded by individual donations. If you would like to support the Network and the LymeNet system of Web services, please send your donations to:
The
Lyme Disease Network of New Jersey 907 Pebble Creek Court,
Pennington,
NJ08534USA http://www.lymenet.org/
UBBFriend: Email this page to someone!
![[Roll Eyes]](rolleyes.gif)
![[bonk]](graemlins/bonk.gif)
Printer-friendly view of this topic